Q65term | Khc-PA
Reported base location of mutation is relative to noncoding strand.
adult cuticle & scutellar bristle | somatic clone
eye photoreceptor cell & endoplasmic reticulum | somatic clone
eye photoreceptor cell & multivesicular body | somatic clone
follicle cell & mitochondrion | germ-line clone
germline cyst & mitochondrion | germ-line clone
microtubule & oocyte | oogenesis stage S9 | germ-line clone
Aplip1EK4/+; Khc27/+ larvae show posterior paralysis in 86% of cases; these mutants also show axonal swelling. Expression of the Aplip1+tHa transgene fully rescues the posterior paralysis phenotype of Aplip1EK4/+; Khc27/+ larvae and partially rescues the axonal swelling phenotype.
The lethality of Khc27 mutant larvae is delayed by Scer\GAL4elav.PLu-driven expression of KhcScer\UAS.P\T.T:Equa\eqFP578-TagBFP2 or KhcmutA.Scer\UAS.P\T.T:Equa\eqFP578-TagBFP2, although the latter is much less effective. All Khc27 mutants die before pupariation regardless of the expression of either of the two transgenes.
Approximately 60% of Khc1-849.αTub67C.T:Avic\GFP mutants oocytes exhibit incorrect nucleus positioning, with the nucleus found separated from the anterior membrane by more than half a nucleus radius.
Approximately 70% of Khc1-700.αTub67C.T:Avic\GFP, Khc27 mutants oocytes exhibit incorrect nucleus positioning, with the nucleus found separated from the anterior membrane by more than half a nucleus radius.
Approximately 33% of Khc1-938.αTub67C.T:Avic\GFP, Khc27 mutants eggs show aberrant nucleus positioning and dorsal appendage formation is strongly affected. These mutants also show the aberrant accumulation of actin-recruiting spheres.